Preliminary studies have shown that Ca ions can reverse the mycardial depression caused by anesthetic agents (halothane and nitrous oxide) in cat papillary muscle. The phasic contraction produced by a 3 msec electrical pulse is more severely depressed by halothane than is the tonic contraction produced by tetanizing the muscle. This suggests actions both at the cell surface and within the cell. Effects of halothane on Ca ions binding by the troponin-tropomyosin complex have been demonstrated by us, but the effect seems to be caused by the surface denaturation of proteins by halothane. Preliminary results suggest that the amount of surface bound Ca ions decreased markedly by 0.5-1% halothane, a result which suggests that the Ca flux during systolics may be reduced by the anesthetic. By low concentration of halothane, Ca-uptake by sarcoplasmic reticulum (SR) decreases, but Ca-release upon depolarization of SR membrane increases. This suggests that SR is another point of attack. We plan to study the effects of anesthetics on: 1) the amount of Ca ions bound at the cell surface using a trivalent cation (lanthanum) which competively displaces membrane bound Ca ions from dog trabecular muscle; 2) Ca ions binding by using isolated plasma membrane preparations and purified calcium binding protein from plasma membrane using arsenazo III and a dual wavelength spectrophotomter; 3) uptake and release of Ca ions by SR by the same method; 4) ATPase activity and the formation and decomposition of phosphorylated intermediates of SR as a method of studying Ca ions transport mechanisms.